The proposed research effort is designed to utilize multidisciplinary techniques in order to examine the hormonal regulation of peripheral autonomic neurons. In so doing these investigations will seek to answer a number of questions generated by testing the fundamental hypothesis that gonadal steroids exert regulatory influences on the growth and development of autonomic neurons and thus hormonal factors determine the biochemical and morphological characteristics of peripheral sympathetic neurons and parasympathetic neurons. The major questions to be answered include: 1) Do gonadal steroids influence both neurochemical (cholinergic and noradrenergic) and morphological (cell number, size, etc.) characteristics of ganglia? 2) Is there a critical time during which these hormonal factors are operative and do androgens and/or estrogens mediate these effects? 3) Do hormones exert their effects directly (i.e., are there androgen receptors in ganglia) or does testosterone regulate the target organ which in turn indirectly influences the neuron, or do both mechanisms exist? 4) Do hormonal factors regulate sympathetic maturation prenatally as well as postnatally. 5) Are similar regulatory influences operative in peripheral parasympathetic ganglia? This project will utilize well established biochemical, pharmacological, morphological, and microneurosurgical techniques in order to address the aforementioned hypothesis and questions. These pursuits will hopefully permit the development of new understandings of the manner and mechanisms by which endocrinological factors influence neuronal ontogeny, thus expanding our understanding of neuroendocrinological interactions during growth and development. Furthermore, such developmental studies may determine how prenatal and postnatal environmental factors alter ontogeny and result in developmental deficits. Accordingly, these experiments may bear upon birth defects secondary to perinatal injuries and pharmacological interactions and such specific developmental disorders as familial dysautono mia (Riley-Day Syndrome).